This is hard to estimate, because it depends on the distribution of effects across the genome, and also on the excess purchase Fostamatinib variation in estimates due to LD in the founder population.However, we note that if the effect of this locus is large enough that it would certainly be detected in this study, then there is no estimation bias from this buy Fostamatinib source.We also assume that there are two haplotypes, each with a definite effect.There might in fact be heterogeneity in the effects of each haplotype, for two reasons.First, this region might have had heterogeneous effects in the founder population, with multiple alleles at multiple causal loci.Second, as recombination breaks up the founder genomes, blocks of genome would become associated with different backgrounds.To the extent that genetic variation is spread evenly over an infinitesimal background, this latter effect is accounted for by our simulations, and has little consequence.However, we have not tested whether the data might be explained by more than two alleles, possibly at more than one discrete locus.Testing such complex models would be challenging, and we do not believe that such test would have much power.However, the estimates of selection made here should be regarded as effective values that may reflect a more complex reality.figure supplement A.However, the exact effect of the allele is difficult to pinpoint in any given generation or population due the nature of the composite trait and change in variance in the composite trait over generations.figure supplement. Artificial selection allowed detailed reconstruction of selection parameters.Rapid response to selection produced mice with progressively longer tibiae within generations.Having complete records throughout the selection experiment makes it possible to reconstruct the selection response for both phenotypes and genotypes in detail.Trajectory in selection response shows decoupling of correlation between tibia length and body mass.In each simulated family, offsprings are split by sex and ranked by their simulation.We vary to find the value where actual breeders composite trait.Open dots show replicate simulations, made with the same pedigree and the same selection actual map length of each of the mouse chromosomes. The simulation agrees well with the observed genomewide average.We simulate founder haplotypes that are consistent with observed genotypes by directly sampling from founder individuals in each LS line.This produces founder haplotypes that carry no linkage disequilibrium. Under the random assignment scheme, we sample according to each individual. At heterozygote sites in each individual, we randomly assign the alleles to the two haplotypes.This produces founder haplotypes that show minimal LD that is consistent with the observed genotypes. Under the max LD assignment scheme, we also sample according to each individual, except that we consistently assign its haplotypes and with reference alleles, respectively.The distribution of minor allele frequencies q at generation is black line shows the diffusion limit, calculated for scaled time, with estimated to compared with the distribution expected with no selection, given a frequency of, or minor alleles out of founding alleles.Significance threshold values under varying LD from simulated replicates. This is because weak associations between large numbers of SNP can greatly inflate the variance of z.